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目的探讨小檗碱对NIT-1细胞胰岛素分泌的影响及可能的作用机制。方法采用小檗碱干预后,用MTT法、放射免疫法及Western blotting确定小檗碱干预的合适浓度范围及检测NIT-1细胞胰岛素水平和腺苷酸活化蛋白激酶(AMP-activated protein kinase,AMPK)蛋白的表达。结果小檗碱在浓度为100μmol/L时对基础培养基和高糖培养基干预的NIT-1细胞的增殖存在显著性抑制作用(P<0.05);而小檗碱在浓度为30μmol/L时就明显抑制高脂培养基诱导的NIT-1细胞的增殖(P<0.05)。小檗碱分别对基础、高糖和高脂诱导的NIT-1细胞短时相干预(1 h)后,显示葡萄糖刺激胰岛素分泌(GSIS)被明显抑制(P<0.05);小檗碱对高糖高脂诱导的NIT-1细胞长时相干预(24 h)后显示基础胰岛素分泌和GSIS均有一定的增加(P<0.05,P<0.01)。小檗碱可以促进高糖高脂诱导的NIT-1细胞AMPK蛋白的表达。结论小檗碱不仅仅作为一种AMPK激活来调节胰岛素分泌,其也可能通过其他的通路进一步影响胰岛素分泌。
Objective To investigate the effect of berberine on insulin secretion and its possible mechanism in NIT-1 cells. Methods The berberine intervention was used to determine the appropriate concentration range of berberine intervention and detect the insulin level and AMP-activated protein kinase (AMPK) in NIT-1 cells by MTT, radioimmunoassay and Western blotting. ) Protein expression. Results Berberine inhibited the proliferation of NIT-1 cells pretreated with basal medium and high glucose medium at the concentration of 100 μmol / L (P <0.05), while at the concentration of 30 μmol / L, berberine Significantly inhibited the proliferation of NIT-1 cells induced by high-fat medium (P <0.05). Berberine inhibited glucose uptake (GSIS) significantly (P <0.05) after a short period of 1 h exposure to NIT-1 cells induced by basal, hyperglycemia and hyperlipidemia, respectively. Glucose-induced long-term NIT-1 cells (24 h) showed basal insulin secretion and increased GSIS (P <0.05, P <0.01). Berberine can promote high glucose and lipid-induced AMPK protein expression in NIT-1 cells. Conclusion Berberine not only regulates insulin secretion as an AMPK activation but may also further affect insulin secretion through other pathways.